The primary objectives of this proposal are 1) to determine whether edema formation occuring after re-expansion of chronically collapsed lung is due to a) altered alveolar-capillary membrane permeability to solvent and macromolecules or b) elevation of the hydrostatic gradient of pressure between the pulmonary microvasculature and interstitial spaces. "Chronic" collapse of rabbit lungs will be maintained for 8 days by daily injection of air into the pleural space. Permeability of the alveolar-capillary membrane will be assessed by measurement of diffusion rates of electrolyte (Na) protein, and dextrans (polyvinyl pyrrolidine) from blood into the interstitial and alveolar spaces. The role of a more negative interstitial pressure will be evaluated by measurement of intravascular, interstitial, and intrapleural pressure in atelectatic lungs before, during, and after re-inflation. Surface forces and tissue compliance, which may effect interstitial pressure in the lung by altering its recoil properties will be assessed by performing static pressure-volume curves with air and saline in chronically collapsed lungs.